Objective: The objective of this study was to conduct a systematic review and meta‐analysis of intervention trials that have determined the effect of unprocessed red meat (URM) intake on obesity‐related outcomes. Methods: The populations, interventions, controls, and outcomes (PICO) framework was used to create questions to search seven databases from July 29, 2020, to August 21, 2020. Two reviewers independently screened 5630 references. English‐language intervention trials in adults testing the effect of URM on obesity‐related outcomes were included. Twenty‐four studies met selection criteria. A random‐effects model was developed to calculate pooled effect sizes. The DerSimonian‐Laird estimator was used to estimate the variance of the true effect sizes. An interactive dashboard was published to provide transparent analysis and data presentation. Results: We found no significant effect of URM for BMI, body weight, or percent body fat based on unfiltered pooled effect sizes. Filtered pooled effect size analysis showed a slight adverse effect of URM for total cholesterol and low‐density lipoprotein cholesterol. Conclusions: Studies did not show an effect of URM on weight gain, obesity, or related metabolic conditions. This may help clinicians when considering the use of URM for patients. Longer studies may be needed for observing obesity development in case the effect of URM on weight gain is small and needs a much longer time to express.

Primary liver cancer, particularly hepatocellular carcinoma (HCC), remains a major global health burden, ranking as the fifth most common cancer and the third leading cause of cancer-related mortality worldwide. The rising incidence of HCC is closely linked to metabolic comorbidities, including non-alcoholic fatty liver disease (NAFLD), underscoring the need for improved diagnostic and therapeutic strategies. NAFLD can progress to metabolic dysfunction-associated steatohepatitis (MASH), characterized by inflammation and fibrosis, which markedly increases HCC risk, especially in individuals with obesity and type 2 diabetes (T2D). NAFLD has recently been redefined as metabolic dysfunction-associated steatotic liver disease (MASLD) to better reflect its metabolic basis. However, robust experimental models to study the progression from MASLD to MASH and ultimately HCC remain limited. This proof-of-concept study investigates sex-specific effects of metabolic dysregulation using the STAM (STelic Animal Model; streptozotocin and high-fat diet) mouse model, which recapitulates key features of human MASH and HCC. Neonatal C57BL/6J mice received streptozotocin to induce T2D-like symptoms followed by a high-fat diet. Streptozotocin (STZ) treated mice showed reduced body fat, lower insulin levels, impaired glucose tolerance, and increased expression of genes linked to inflammation, lipid metabolism, and apoptosis. These findings support the STAM model’s utility for MASLD research and highlight the importance of sex-specific strategies to limit HCC progression.